Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats
- Autores
- Rodriguez, Jesica S.; Vélez Rueda, Jorge Omar; Salas, Margarita Ana; Becerra, Romina Valeria; Di Carlo, Mariano Nahuel; Said, María Matilde; Vittone, Leticia; Rinaldi, Gustavo; Portiansky, Enrique Leo; Mundiña-Weilenmann, Cecilia; Palomeque, Julieta; Mattiazzi, Alicia Ramona
- Año de publicación
- 2014
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca 2+-handling alterations are known to occur in SHR. However, the putative modifications of Ca2+-handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca 2+, Ca2+-handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+/Ca2+ exchanger (NCX) abundance (p< 0.05) with no changes in SERCA2a expression/activity. An increased Ca 2+-calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+-handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident.
Centro de Investigaciones Cardiovasculares
Facultad de Ciencias Veterinarias - Materia
-
Ciencias Médicas
Intercambiador de Sodio-Calcio
Hipertensión - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by-nc-sa/4.0/
- Repositorio
.jpg)
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/85568
Ver los metadatos del registro completo
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Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive ratsRodriguez, Jesica S.Vélez Rueda, Jorge OmarSalas, Margarita AnaBecerra, Romina ValeriaDi Carlo, Mariano NahuelSaid, María MatildeVittone, LeticiaRinaldi, GustavoPortiansky, Enrique LeoMundiña-Weilenmann, CeciliaPalomeque, JulietaMattiazzi, Alicia RamonaCiencias MédicasIntercambiador de Sodio-CalcioHipertensiónSpontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca 2+-handling alterations are known to occur in SHR. However, the putative modifications of Ca2+-handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca 2+, Ca2+-handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+/Ca2+ exchanger (NCX) abundance (p< 0.05) with no changes in SERCA2a expression/activity. An increased Ca 2+-calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+-handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident.Centro de Investigaciones CardiovascularesFacultad de Ciencias Veterinarias2014info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/85568enginfo:eu-repo/semantics/altIdentifier/issn/1932-6203info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0096400info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:16:21Zoai:sedici.unlp.edu.ar:10915/85568Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:16:21.326SEDICI (UNLP) - Universidad Nacional de La Platafalse |
| dc.title.none.fl_str_mv |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| title |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| spellingShingle |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats Rodriguez, Jesica S. Ciencias Médicas Intercambiador de Sodio-Calcio Hipertensión |
| title_short |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| title_full |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| title_fullStr |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| title_full_unstemmed |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| title_sort |
Increased Na+/Ca2+ exchanger expression/activity constitutes a point of inflection in the progression to heart failure of hypertensive rats |
| dc.creator.none.fl_str_mv |
Rodriguez, Jesica S. Vélez Rueda, Jorge Omar Salas, Margarita Ana Becerra, Romina Valeria Di Carlo, Mariano Nahuel Said, María Matilde Vittone, Leticia Rinaldi, Gustavo Portiansky, Enrique Leo Mundiña-Weilenmann, Cecilia Palomeque, Julieta Mattiazzi, Alicia Ramona |
| author |
Rodriguez, Jesica S. |
| author_facet |
Rodriguez, Jesica S. Vélez Rueda, Jorge Omar Salas, Margarita Ana Becerra, Romina Valeria Di Carlo, Mariano Nahuel Said, María Matilde Vittone, Leticia Rinaldi, Gustavo Portiansky, Enrique Leo Mundiña-Weilenmann, Cecilia Palomeque, Julieta Mattiazzi, Alicia Ramona |
| author_role |
author |
| author2 |
Vélez Rueda, Jorge Omar Salas, Margarita Ana Becerra, Romina Valeria Di Carlo, Mariano Nahuel Said, María Matilde Vittone, Leticia Rinaldi, Gustavo Portiansky, Enrique Leo Mundiña-Weilenmann, Cecilia Palomeque, Julieta Mattiazzi, Alicia Ramona |
| author2_role |
author author author author author author author author author author author |
| dc.subject.none.fl_str_mv |
Ciencias Médicas Intercambiador de Sodio-Calcio Hipertensión |
| topic |
Ciencias Médicas Intercambiador de Sodio-Calcio Hipertensión |
| dc.description.none.fl_txt_mv |
Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca 2+-handling alterations are known to occur in SHR. However, the putative modifications of Ca2+-handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca 2+, Ca2+-handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+/Ca2+ exchanger (NCX) abundance (p< 0.05) with no changes in SERCA2a expression/activity. An increased Ca 2+-calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+-handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident. Centro de Investigaciones Cardiovasculares Facultad de Ciencias Veterinarias |
| description |
Spontaneously hypertensive rat (SHR) constitutes a genetic model widely used to study the natural evolution of hypertensive heart disease. Ca 2+-handling alterations are known to occur in SHR. However, the putative modifications of Ca2+-handling proteins during the progression to heart failure (HF) are not well established. Moreover, the role of apoptosis in SHR is controversial. We investigated intracellular Ca 2+, Ca2+-handling proteins and apoptosis in SHR vs. control Wistar rats (W) from 3 to 15 months (mo). Changes associated with the transition to HF (i.e. lung edema and decrease in midwall fractional shortening), occurred at 15 mo in 38% of SHR (SHRF). In SHRF, twitch and caffeine-induced Ca2+ transients, significantly decreased relative to 6/9 mo and 15 mo without HF signs. This decrease occurred in association with a decrease in the time constant of caffeine-Ca2+ transient decay and an increase in Na+/Ca2+ exchanger (NCX) abundance (p< 0.05) with no changes in SERCA2a expression/activity. An increased Ca 2+-calmodulin-kinase II activity, associated with an enhancement of apoptosis (TUNEL and Bax/Bcl2) was observed in SHR relative to W from 3 to 15 mo. Conclusions: 1. Apoptosis is an early and persistent event that may contribute to hypertrophic remodeling but would not participate in the contractile impairment of SHRF. 2. The increase in NCX expression/activity, associated with an increase in Ca2+ efflux from the cell, constitutes a primary alteration of Ca2+-handling proteins in the evolution to HF. 3. No changes in SERCA2a expression/activity are observed when HF signs become evident. |
| publishDate |
2014 |
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2014 |
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eng |
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